Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The etiology of the atherosclerosis that occurs in diabetes mellitus is unclear. Adenosine has been shown to inhibit growth of rat aortic smooth muscle cells. Nucleoside transporters play an integral role in adenosine function by regulating adenosine levels in the vicinity of adenosine receptors. Therefore, we studied the effect of 25 mM d-glucose, which mimics hyperglycemia of diabetes, on adenosine transport in cultured human aortic smooth muscle cells (HASMCs). Although RT-PCR demonstrated the presence of equilibrative nucleoside transporter-1 (ENT-1) and ENT-2 mRNA, functional studies revealed that adenosine transport in HASMCs was predominantly mediated by ENT-1 and inhibited by nitrobenzylmercaptopurine riboside (NBMPR, IC(50) = 0.69 +/- 0.05 nM). Adenosine transport in HASMCs was increased by >30% after treatment for 48 h with 25 mM d-glucose, but not with equimolar d-mannitol and l-glucose. Kinetic studies showed that d-glucose increased V(max) of adenosine transport without affecting K(m). Similarly, d-glucose increased B(max) of high-affinity [(3)H]NBMPR binding, while the dissociation constant (K(d)) was not changed. Consistent with these observations, 25 mM d-glucose increased mRNA and protein expression of ENT-1. Treatment of serum-starved cells with the selective inhibitors of MAPK/ERK, PD-98059 (40 microM) and U-0126 (10 microM), abolished the effect of d-glucose on ENT-1. We conclude that d-glucose upregulates the protein and message expression and functional activity of ENT-1 in HASMCs, possibly via MAPK/ERK-dependent pathways. Pathologically, the increase in ENT-1 activity in diabetes may affect the availability of adenosine in the vicinity of adenosine receptors and, thus, alter vascular functions in diabetes.
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PMID:D-Glucose upregulates adenosine transport in cultured human aortic smooth muscle cells. 1569 55

A 49-year old employee of a drug store with neck pain, painful thyroid gland, and elevated erythrocyte sedimentation rate (38 mm/h) was diagnosed as subacute thyreoiditis (de Quervain). However, application of oral corticosteroids (prednisone 50 mg/d) during three days did not reduce pain as expected. Therefore, the patient was admitted for further evaluation. Clinical examination showed a female in a pain-relieving posture (forward neck flexion). Further examinations including ultrasound of the thyroid, computertomography of the neck, and ENT examination did not reveal etiology of the pain. Finally, electrocardiography showed subacute infero-posterior myocardial infarction, and coronary angiography revealed severe coronary two vessel disease. Tabacco smoking since the age of fourteen (35 pack years) was identified as the only major risk factor for premature atherosclerosis. Diagnosis of subacute thyreoiditis is made from clinical and laboratory findings. Treatment with nonsteroidal antiinflammatory drugs or corticosteroids usually relieves pain within two or three days. Otherwise, etiology of the disease must be re-evaluated considering any disease localized in neck or thorax region. Antiinflammatory treatment of subacute thyreoiditis has to be continued for weeks or months.
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PMID:["Subacute thyreoiditis" without response on corticosteroid therapy]. 1594 Sep 11

Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of NO synthetase. Elevated ADMA levels are accompanied by impaired endothelium-dependent vasodilation in the brachial artery and increased intima-media thickness in the elastic arteries. The purpose of the study was to develop a procedure for qualitative and quantitative determination of the plasma content of free ADMA and symmetric dimethylarginine by reverse-phase high performance liquid chromatography in an isocratic elution mode, by applying an electrochemical detector. Ortho-phthalic aldehyde with the sulfur-containing component sodium sulfite was used as a derivation reagent. The mobile phase is a system that consists of acetonitrile, sodium hydrophosphate, and sodium dihydrophosphate. The retention time for the detectable substance on the column was 21.7 min. The total time of the analysis was 31 min. In patients with the clinical manifestations of atherosclerosis and in healthy individuals, the plasma ADMA concentration measured by the devised method was 0.69-0.30 and 0.13-0.04 microM, respectively.
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PMID:[Determination of human plasma concentration of asymmetric dimethylarginine by high performance liquid chromatography using an electrochemical detector]. 2060 47

Neutrophil extracellular traps represent a fascinating mechanism by which PMNs entrap extracellular microbes. The primary purpose of this innate immune mechanism is thought to localize the infection at an early stage. Interestingly, the ability of different microcrystals to induce NET formation has been recently described. Microcrystals are insoluble crystals with a size of 1-100 micrometers that have different composition and shape. Microcrystals have it in common that they irritate phagocytes including PMNs and typically trigger an inflammatory response. This review is the first to summarize observations with regard to PMN activation and NET release induced by microcrystals. Gout-causing monosodium urate crystals, pseudogout-causing calcium pyrophosphate dehydrate crystals, cholesterol crystals associated with atherosclerosis, silicosis-causing silica crystals, and adjuvant alum crystals are discussed.
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PMID:Neutrophil Extracellular Traps and Microcrystals. 2837 94


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